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A 29-Year-Old Man Presented to the Dermatology Clinic with a Pruritic, Erythematous, and Scaly Rash That Had First Appeared 2 Years Earlier

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A 29-Year-Old Man Presented to the Dermatology Clinic with a Pruritic, Erythematous, and Scaly Rash That Had First Appeared 2 Years Earlier A 29-year-old man presented to the dermatology clinic with a pruritic, erythematous, and scaly rash that had first appeared 2 years earlier. He had sought no medical treatment until this presentation. His medical history included eczema during childhood and seasonal allergies. Physical examination showed erythematous, violaceous plaques that involved more than 90% of the patient’s body-surface area, with some areas that were spared and reflect the baseline appearance of the patient’s skin. What is the diagnosis? Seborrheic dermatitis The answer is erythrodermic psoriasis. The differential Pityriasis rubra pilaris diagnosis for generalized erythema and plaque formation includes erythrodermic psoriasis, seborrheic Erytherma multiforme dermatitis, and pityriasis rubra pilaris. A punch biopsy specimen obtained from two areas on the back Erythrodermic psoriasis confirmed the diagnosis of erythrodermic psoriasis. An erythrodermic papulosquamous eruption can be Toxic Epidermal Necrolysis associated with an underlying systemic disease. In this case, testing for human immunodeficiency virus (HIV) infection was positive. Psoriatic erythroderma (also known as erythrodermic psoriasis) represents a generalized form of psoriasis that affects all body sites, including the face, hands, feet, nails, trunk, and extremities. First-line treatments for psoriatic erythroderma include immunosuppressive medications such as methotrexate, acitretin, or ciclosporin. Erythroderma is a generalised redness of the skin. It is a very severe skin condition that can be fatal. It can be the result of many inflammatory skin conditions, drugs and malignancies but in a third of cases it is due to psoriasis. Erythrodermic psoriasis may be precipitated by: Infections Low calcium Withdrawal of oral corticosteroids (prednisone) Withdrawal of excessive use of strong topical corticosteroids Strong coal tar preparations Certain medications including lithium, antimalarials and interleukin II Excessive alcohol consumption Erythrodermic psoriasis usually occurs in the setting of known worsening or unstable psoriasis but may uncommonly be the first presentation of psoriasis. Onset can occur acutely over a few days or weeks, or gradually evolve over several months from pre-existing psoriasis. Als Seborrhoisches Ekzem oder Seborrhoische Dermatitis oder Morbus Unna wird ein Hautausschlag (Ekzem) bezeichnet, der besonders auf der Kopfhaut und im Gesicht auftritt und meist mit Schuppungen verbunden ist. Die spezielle Form des Ausschlags bei Neugeborenen ist unter dem volkstümlichen Namen Grind oder Kopfgneis bekannt und wird häufig mit Milchschorf verwechselt oder mit diesem gleichgesetzt. Es entsteht ein Hautausschlag (häufig mit gelblichen Schuppen), der die behaarte Kopfhaut (Gneis) und angrenzende Bereiche, die Haut um die Nase, das Kinn, die Augenbrauen, die Augenlider und die Haut um die Ohren betreffen kann. In schweren Fällen können auch das Brustbein und der Rücken entlang der Wirbelsäule betroffen sein. Ein starker Juckreiz kann auftreten, aber auch völlig fehlen. Durch Kratzen kann die geschwächte Haut verletzt werden und sich zusätzlich entzünden und bluten. Eine zusätzliche bakterielle Besiedlung ist möglich. Die betroffenen Stellen können kosmetisch sehr beeinträchtigen, verheilen aber in aller Regel ohne Narbenbildung. Die Pathogenese des Seborrhoischen Ekzems ist nicht vollständig geklärt. Es werden mehrere Ursachen angenommen. Eine Hauptursache kann eine erhöhte Talgproduktion und die dadurch bedingte Zunahme der Besiedlung mit Malassezia-Hefen sein. Man ging davon aus, dass die Hautausschläge eine Reaktion auf Stoffwechselprodukte des Hefepilzes Malassezia furfur (vormals Pityrosporum ovale genannt) sind. Inzwischen ist bekannt, dass mehrere Malassezia-Hefen beteiligt sind. Die Pityriasis rubra pilaris (auch Stachelflechte oder Devergie-Krankheit) ist eine seltene chronische Hauterkrankung, die von den Haarfollikeln ausgeht. Die Ursache ist unbekannt. Das Aussehen dieser weitgehend schmerzlosen Erkrankung ähnelt dem der Schuppenflechte (Psoriasis). Die Häufigkeit wird mit unter 1 zu 1.000.000 angegeben, die meisten Fälle treten sporadisch auf, es gibt aber auch familiäre Formen (Devergie-Krankheit) mit autosomal- dominantem Erbgang. Der Erkrankung liegen Mutationen im CARD14-Gen am Genort 17q25.3 zugrunde. Nach dem zu Beginn (an Kopfhaut, Armen und Beinen) schubhaften Auftreten von kleinen orangeroten follikulären Papeln (kleine Knötchen) bilden sich gelbrote flächenhafte und manchmal schuppende Herde. Diese können zu einer Rötung der gesamten Haut führen (Erythrodermie). Ferner findet sich eine palmoplantare-Hyperkeratose. Ein typisches Zeichen für die Pityriasis rubra pilaris sind Inseln von nichtbefallener Haut zwischen den Herden. Ohne Therapie besteht die Erkrankung über Jahre, heilt schließlich aber aus. Die Behandlung mit Etretin führt zum Abblassen und Abflachen der Herde innerhalb von wenigen Wochen. Die völlige Heilung dauert jedoch Monate. Erythema (exsudativum) multiforme beschreibt eine akute entzündliche Erkrankung der Haut oder Schleimhaut. Oft tritt diese Hautkrankheit 1–2 Wochen nach einer Infektion auf. Das deutet auf eine immunologische Reaktion hin. Ursache kann auch eine Reaktion auf bestimmte Schadstoffe und Konservierungsmittel (z. B. Triclocarban) sein. Rezidive sind häufig. Es kann auch zu schmerzhaften Schwellungen der Gelenke kommen. Hier hat sich ein Antihistamin (z. B. Fenistil Gel) bewährt. Es existieren zwei Formen: Erythema multiforme minor: typische Hautherde mit fehlender/schwacher Blasenkomponente, meist am Handrücken oder Unterarm. Erythema multiforme major: typische Hautherde mit generalisierter mittiger Blasenbildung (Kokarde) inklusive der Füße und Handinnenflächen, diese imponieren als sogenannte „Schießscheibenläsionen“. Es kann zu Erosionen der Mundschleimhaut und schwerem Hautbefall kommen. Auslöser können sowohl verschiedene Viren (z. B. Herpes-simplex- Viren) wie auch verschiedene Arzneimittel sein. Es herrscht ein fließender Übergang zum Stevens- Johnson-Syndrom. Linderung bringen Kühlung (Kühlpads, feuchte Wickel) und Schmerzmittel. Ggf. kann ein Antiallergikum (z. B. Cetirizin) schnelle Abhilfe schaffen. Das Lyell-Syndrom, auch als Epidermolysis acuta toxica oder Syndrom der verbrühten Haut bezeichnet, ist eine seltene, nach dem schottischen Dermatologen Alan Lyell benannte akute Hautveränderung, die durch blasige Ablösungen der Epidermis der Haut („Syndrom der verbrühten Haut“) gekennzeichnet ist. Die Sterblichkeitsrate beträgt je nach Ausmaß der Schädigung zwischen 25 und 70 %. Es gibt zwei Formen des Lyell-Syndroms. Das medikamentös induzierte Lyell-Syndrom (Toxische epidermale Nekrolyse, TEN) und das staphylogene Lyell-Syndrom (Staphylococcal scalded skin syndrome, SSSS). Das medikamentös induzierte Lyell-Syndrom tritt als zytotoxische allergische Reaktion auf Medikamente insbesondere bei Erwachsenen, seltener bei Kindern auf. Aufgrund der sehr ähnlichen Klinik und Histopathologie kann die TEN als Maximalform des Stevens-Johnson-Syndroms angesehen werden. Folgende Medikamente gelten nach Angaben der Arzneimittelkommission der deutschen Ärzteschaft als mögliche Auslöser: antibakterielle Sulfonamide, zum Beispiel Cotrimoxazol (Mischung aus Sulfamethoxazol und Trimethoprim) Antikonvulsiva, zum Beispiel Phenytoin, Carbamazepin, Lamotrigin Analgetika und nichtsteroidale Antirheumatika, vor allem Pyrazolone wie Metamizol Allopurinol. Das Ovarialkarzinom oder Eierstockkrebs ist eine bösartige Erkrankung der Eierstöcke. Es ist in der westlichen Welt nach dem Endometrium- und dem Zervixkarzinom das dritthäufigste Genitalmalignom der Frau und hat eine schlechtere Prognose als jene. Das mittlere Erkrankungsalter beträgt in Deutschland 69 Jahre, wobei auch wesentlich jüngere Frauen, dann häufig in Zusammenhang mit genetischer Prädisposition, erkranken können. Frauen in Deutschland haben ein Lebenszeitrisiko von 1,5 %, an Eierstockkrebs zu erkranken. Die Inzidenz des Ovarialkarzinoms ist in den letzten 20 Jahren deutlich gesunken, wohingegen die Mortalitätsraten sich auf einem etwa konstanten Niveau bewegen. Von 2005 bis 2009 fielen die alters- und bevölkerungskorrigierten Inzidenzraten bundesweit von 13,5 auf 11,5 Neuerkrankungen pro 100.000 weiblichen Einwohnern und Jahr. Die geschätzten Inzidenzraten für das Jahr 2012 lassen 7.200 Neuerkrankungsfälle erwarten, was einer alters- und bevölkerungskorrigierten Inzidenzrate von 11,0 neuen Fällen pro 100.000 weiblichen Einwohnern entspricht. Die Erkrankung tritt familiär gehäuft auf. Die beiden Gene BRCA1 und BRCA2 spielen (wie beim Brustkrebs) eine Rolle. Kinderlose und Spätgebärende haben gegenüber der Normalbevölkerung ein 2,5-fach erhöhtes Risiko, daran zu erkranken. Hormonelle Kontrazeptiva, häufige Schwangerschaften und langes Stillen sind dagegen protektive Faktoren, da die Eierstöcke durch sie „ruhiggestellt“ werden. Poly(ADP-Ribose)-Polymerase 1 (PARP-1) ist ein körpereigenes Enzym, welches an der DNA- Reparatur beteiligt ist. Die Hemmung des Enzyms führt dazu, dass Brüche in einzelsträngiger DNA (ssDNA) nur noch mithilfe homologer Rekombination behoben werden können. Daher können möglicherweise Krebszellen, bei denen häufig die homologe Rekombination defekt ist, mit Substanzen, die PARP-1 hemmen, abgetötet werden. Der proteolytische Abbau von PARP-1 durch Caspase-3 ist ein Zwischenschritt des programmierten Zelltods (Apoptose). In verschiedenen Spezies ist die Langlebigkeit von Zellen mit der PARP-1-Aktivität korreliert. Auch ist PARP-1 in Neuronen aktiv, die
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